Turner J R, Tartakoff A M
Institute of Pathology, Case Western Reserve University, Cleveland, Ohio 44106.
J Cell Biol. 1989 Nov;109(5):2081-8. doi: 10.1083/jcb.109.5.2081.
A striking example of the interrelation between the Golgi complex (GC) and microtubules is the reversible fragmentation and dispersal of the GC which occurs upon microtubule depolymerization. We have characterized dispersal of the GC after nocodazole treatment as well as its recovery from the dispersed state by immunofluorescent localization of beta 1, 4-galactosyltransferase in Madin-Darby bovine kidney cells. Immunofluorescent anti-tubulin staining allowed simultaneous examination of the microtubule array. Based on our results, dispersal can be divided into a three-step process: microtubule depolymerization, GC fragmentation, and fragment dispersal. In cells treated with metabolic inhibitors after microtubule depolymerization, neither fragmentation nor dispersal occur, despite the absence of assembled microtubules. Thus, fragmentation is energy dependent and not tightly linked to microtubule depolymerization. The slowing of fragmentation and dispersal by monensin or ammonium chloride, as well as progressive inhibition at less than 34 degrees C, suggest that ongoing membrane traffic is required for these processes. Similarly, recovery may be separated into four steps: microtubule depolymerization, GC fragment centralization, fragment coalescence, and polarization of the reticular GC network. Fragment centralization and coalescence were arrested by metabolic inhibitors, despite the presence of microtubules. Neither monensin nor ammonium choride inhibited GC recovery. Partial inhibition of recovery at reduced temperatures paralleled the extent of microtubule assembly. These data demonstrate that dispersal and recovery are multi-step operations, and that the individual steps differ in temperature dependence, energy dependence, and sensitivity to ionic perturbation. GC distribution and microtubule status have also been clearly dissociate, thereby proving that organization of the GC is an active process that is not simply determined by microtubule binding. Furthermore, the results indicate that ongoing intra-GC membrane traffic may participate in fragmentation and dispersal.
高尔基体复合体(GC)与微管之间相互关系的一个显著例子是,微管解聚时GC会发生可逆的碎片化和分散。我们通过对Madin-Darby牛肾细胞中β1,4-半乳糖基转移酶进行免疫荧光定位,对诺考达唑处理后GC的分散情况及其从分散状态的恢复进行了表征。免疫荧光抗微管蛋白染色可同时检测微管阵列。根据我们的结果,分散可分为三个步骤:微管解聚、GC碎片化和片段分散。在微管解聚后用代谢抑制剂处理的细胞中,尽管没有组装好的微管,但既不发生碎片化也不发生分散。因此,碎片化是能量依赖的,与微管解聚没有紧密联系。莫能菌素或氯化铵使碎片化和分散减缓,以及在低于34摄氏度时逐渐受到抑制,表明这些过程需要持续的膜运输。同样,恢复可分为四个步骤:微管解聚、GC片段集中化、片段合并以及网状GC网络的极化。尽管存在微管,但代谢抑制剂阻止了片段集中化和合并。莫能菌素和氯化铵均未抑制GC的恢复。在降低温度下对恢复的部分抑制与微管组装程度平行。这些数据表明,分散和恢复是多步骤操作,且各个步骤在温度依赖性、能量依赖性和对离子扰动的敏感性方面存在差异。GC分布和微管状态也已明显分离,从而证明GC的组织是一个活跃过程,并非简单地由微管结合决定。此外,结果表明GC内持续的膜运输可能参与碎片化和分散。